Heart failure is a growing and dominant public health problem in the United States. Literally, millions of patients in this country suffer from heart failure and more than half a million patients are newly diagnosed with heart failure every year. The heart failure patient pool is continuing to grow at an increasing rate partly because of early recognition and better treatment coupled with “salvage” of patients with acute myocardial infarctions earlier in life. Heart failure is the most common Medicare DRG group and more Medicare dollars are spent for the diagnosis and treatment of heart failure than for any other diagnosis. The costs of heart failure treatment can be dramatically reduced by decreasing hospital stay alone.
The patho-physiology of heart failure involves changes in cardiac function, neuro-humoral status, blood volumes, and systemic vascular resistance. A primary change in cardiac function precipitates changes in neuro-humoral status, blood volume and vascular resistance. These changes can neutralize cardiac dysfunction up to certain limits. Therefore, some of the most effective conventional treatments for chronic heart failure involve modulating non-cardiac factors such as modifying renal and vascular function.
In regard to cardiac changes, systolic dysfunction, diastolic dysfunction, or combination of both can result in decline in stroke volume. Ischemic cardiomyopathy is the most common cause of chronic heart failure. For neuro-humeral changes, arterial and venous vasoconstriction and increases in blood volume, as a result of sympathetic activation and renin-angiotensin system, increased anti-diuretic hormone/vasopressin, and atrial-natriuretic peptide, try to compensate for the decline in cardiac output. However, this paradoxically affects cardiac function further by increasing both ventricular afterload and preload. Factors such as nitric oxide and endothelin, both of which are increased in heart failure, may play a role in the pathogenesis of heart failure. GFR becomes dependent on afferent arteriolar flow in the most severe heart failure, despite stimulation of hormonal and homodynamic pathways, which would normally increase efferent arteriolar tone.
Arterial and venous constriction as a result of sympathetic activation is also enhanced by humoral activation via, for example, the renin-angiotensin system and antidiuretic hormones, such as, for example, vasopressin. Further, a compensatory increase in blood volume serves to increase ventricular preload and thereby enhance stroke volume by the Frank-Starling mechanism.
One will appreciate that blood volume can be augmented by a number of mechanisms. For example, reduction of renal blood flow results in decreased urine output and retention of fluid. Furthermore, a combination of reduced renal perfusion and sympathetic activation of the kidneys activates the renin-angiotensin system, which, in turn, enhances aldosterone secretion. Still further, increases in circulating arginine vasopressin (antidiuretic hormone) contributes to renal retention of water. As a result, final outcome of humoral activation is an increase in renal reabsorption of sodium and water. The resultant increase in blood volume helps to maintain cardiac output; however, this increase can be deleterious because it raises venous pressures, which can lead to pulmonary and systemic edema. FIG. 6 summarizes the compensatory mechanisms described above.
As noted above, it is well known that cardiac dysfunction induces a series of events that ultimately contribute to congestive heart failure. Reductions in renal blood flow due to reduced cardiac output can, in turn, result in the retention of excess fluid in the patient's body, leading for example, to pulmonary and cardiac edema. The vicious cycle of fluid and electrolytes retention increases the work of the compromised heart.
In a healthy adult, kidneys are perfused by about 20 to 22% of cardiac output, which typically results in around 60,000 cc of blood circulating through kidneys per hour. Chapter 62 of Heart Disease: A Textbook of Cardiovascular Medicine, (E. Braunwald, ed., 5th ed. 1996), published by Saunders, Philadelphia, Pa., reports that for patients with congestive heart failure, the fall in effective renal blood flow is proportional to the reduction in cardiac output. Renal blood flow in normal patients in an age range of 20-80 years averages 600 to 660 ml/min/m2, corresponding to about 14 to 20% of simultaneously measured cardiac output. Within a wide spectrum of CHF severity, renal blood flow is depressed to an average range of 250 to 450 ml/min/m2.
Thus, in acute decompensation, it is beneficial to improve renal perfusion. In view of the foregoing, it would be desirable to increase renal profusion by positioning a catheter below the renal artery. This would beneficially result in an increase in laminar flow in the aorta and a decrease in the serum levels of vasoconstrictors. Thus, improvements in renal circulation as well as laminar flow in the aorta can be achieved.
It further would be desirable to provide methods and apparatus for treating and managing heart failure without administering high doses of drugs or dehydrating the patient. It further would be desirable to provide methods and apparatus for treating and managing heart failure by improving blood flow to the kidneys, thereby enhancing renal function. It also would be desirable to provide methods and apparatus for treating and managing heart failure that permit the administration of low doses of drugs, in a localized manner, to improve renal function.